In our earlier work, using a conditional Scn1a knockout model for epilepsy, we showed that selective impairment of θ–low-γ PAC can be explained by selective disruption of hippocampal inhibition.47 The observed impairment of θ–low-γ PAC in our Alzheimer's disease model thereby suggests selective impairment of hippocampal compared to cortical inhibitory neuronal activity and fits with reported reduction in hippocampal PV and SST interneuronal functioning in the context of Alzheimer's disease pathology and memory deficits.31,67,78. Here, SCN1A is linked to epilepsy.